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禽致病性[相关内容未完整]与小鼠微血管内皮细胞系bEnd.3相互作用过程中的转录组分析。

Transcriptome profiling of avian pathogenic and the mouse microvascular endothelial cell line bEnd.3 during interaction.

作者信息

Wang Peili, Meng Xia, Li Jianji, Chen Yanfei, Zhang Dong, Zhong Haoran, Xia Pengpeng, Cui Luying, Zhu Guoqiang, Wang Heng

机构信息

College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, China.

Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, Jiangsu, China.

出版信息

PeerJ. 2020 May 21;8:e9172. doi: 10.7717/peerj.9172. eCollection 2020.

DOI:10.7717/peerj.9172
PMID:32509459
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7246031/
Abstract

BACKGROUND

Avian pathogenic (APEC), an important extraintestinal pathogenic , causes colibacillosis, an acute and mostly systemic disease involving multiple organ lesions such as meningitis. Meningitis-causing APEC can invade the host central nervous system by crossing the blood-brain barrier (BBB), which is a critical step in the development of meningitis. However, the bacteria-host interaction mechanism in this process remains unclear.

METHODS

In this study, we examined and bEnd.3 cells transcriptomes during infection and mock infection to investigate the global transcriptional changes in both organisms using RNA sequencing approach.

RESULTS

When APEC infected the bEnd.3 cells, several significant changes in the expression of genes related to cell junctional complexes, extracellular matrix degradation, actin cytoskeleton rearrangement, immune activation and the inflammatory response in bEnd.3 cells were observed as compared to the mock infection group. Thus, the immune activation of bEnd.3 cells indicated that APEC infection activated host defenses. Furthermore, APEC may exploit cell junction degradation to invade the BBB. In addition, amino acid metabolism and energy metabolism related genes were downregulated and the protein export pathway related genes were upregulated in APEC cultured with bEnd.3 cells, compared to that in control. Thus, APEC may encounter starvation and express virulence factors during incubation with bEnd.3 cells.

CONCLUSION

This study provides a comprehensive overview of transcriptomic changes that occur during APEC infection of bEnd.3 cells, and offers insights into the bacterial invasion strategies and the subsequent host defense mechanism.

摘要

背景

禽致病性大肠杆菌(APEC)是一种重要的肠道外致病性大肠杆菌,可引起大肠杆菌病,这是一种急性且大多为全身性的疾病,会导致包括脑膜炎在内的多个器官损伤。导致脑膜炎的APEC可通过血脑屏障(BBB)侵入宿主中枢神经系统,这是脑膜炎发展过程中的关键步骤。然而,这一过程中细菌与宿主的相互作用机制仍不清楚。

方法

在本研究中,我们检测了感染和模拟感染期间bEnd.3细胞的转录组,以使用RNA测序方法研究两种生物体中的全局转录变化。

结果

与模拟感染组相比,当APEC感染bEnd.3细胞时,观察到bEnd.3细胞中与细胞连接复合体、细胞外基质降解、肌动蛋白细胞骨架重排、免疫激活和炎症反应相关的基因表达发生了一些显著变化。因此,bEnd.3细胞的免疫激活表明APEC感染激活了宿主防御。此外,APEC可能利用细胞连接降解来侵入血脑屏障。此外,与对照组相比,在用bEnd.3细胞培养的APEC中,与氨基酸代谢和能量代谢相关的基因下调,与蛋白质输出途径相关的基因上调。因此,APEC在与bEnd.3细胞共孵育期间可能会遭遇饥饿并表达毒力因子。

结论

本研究全面概述了APEC感染bEnd.3细胞过程中发生的转录组变化,并深入了解了细菌的入侵策略和随后的宿主防御机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43dd/7246031/d0fc2c0da594/peerj-08-9172-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43dd/7246031/8e4de6fc1a21/peerj-08-9172-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43dd/7246031/d0fc2c0da594/peerj-08-9172-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43dd/7246031/8e4de6fc1a21/peerj-08-9172-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43dd/7246031/60c6d77a9477/peerj-08-9172-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43dd/7246031/cf7f3913212a/peerj-08-9172-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43dd/7246031/196cbff402a7/peerj-08-9172-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43dd/7246031/d0fc2c0da594/peerj-08-9172-g005.jpg

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